Combined computational modeling and experimental study of the biomechanical mechanisms of platelet-driven contraction of fibrin clots

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dc.contributor.authorMichael, Christianen
dc.contributor.authorPancaldi, Francescoen
dc.contributor.authorBritton, Samuelen
dc.contributor.authorKim, Oleg V.en
dc.contributor.authorPeshkova, Alina D.en
dc.contributor.authorVo, Khoien
dc.contributor.authorXu, Zhiliangen
dc.contributor.authorLitvinov, Rustem I.en
dc.contributor.authorWeisel, John W.en
dc.contributor.authorAlber, Marken
dc.date.accessioned2023-10-30T12:50:53Zen
dc.date.available2023-10-30T12:50:53Zen
dc.date.issued2023-08-24en
dc.date.updated2023-10-29T20:20:17Zen
dc.description.abstractWhile blood clot formation has been relatively well studied, little is known about the mechanisms underlying the subsequent structural and mechanical clot remodeling called contraction or retraction. Impairment of the clot contraction process is associated with both life-threatening bleeding and thrombotic conditions, such as ischemic stroke, venous thromboembolism, and others. Recently, blood clot contraction was observed to be hindered in patients with COVID-19. A three-dimensional multiscale computational model is developed and used to quantify biomechanical mechanisms of the kinetics of clot contraction driven by platelet-fibrin pulling interactions. These results provide important biological insights into contraction of platelet filopodia, the mechanically active thin protrusions of the plasma membrane, described previously as performing mostly a sensory function. The biomechanical mechanisms and modeling approach described can potentially apply to studying other systems in which cells are embedded in a filamentous network and exert forces on the extracellular matrix modulated by the substrate stiffness.en
dc.description.versionPublished versionen
dc.format.extent16 page(s)en
dc.format.mimetypeapplication/pdfen
dc.identifierARTN 869 (Article number)en
dc.identifier.doihttps://doi.org/10.1038/s42003-023-05240-zen
dc.identifier.eissn2399-3642en
dc.identifier.issn2399-3642en
dc.identifier.issue1en
dc.identifier.other10.1038/s42003-023-05240-z (PII)en
dc.identifier.pmid37620422en
dc.identifier.urihttp://hdl.handle.net/10919/116573en
dc.identifier.volume6en
dc.language.isoenen
dc.publisherNature Portfolioen
dc.relation.urihttps://www.ncbi.nlm.nih.gov/pubmed/37620422en
dc.rightsCreative Commons Attribution 4.0 Internationalen
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/en
dc.subjectBlood clotsen
dc.subject.meshBlood Plateletsen
dc.subject.meshHumansen
dc.subject.meshThrombosisen
dc.subject.meshFibrinen
dc.subject.meshComputer Simulationen
dc.subject.meshCOVID-19en
dc.titleCombined computational modeling and experimental study of the biomechanical mechanisms of platelet-driven contraction of fibrin clotsen
dc.title.serialCommunications Biologyen
dc.typeArticle - Refereeden
dc.type.dcmitypeTexten
dc.type.otherArticleen
dc.type.otherJournalen
dcterms.dateAccepted2023-08-10en
pubs.organisational-group/Virginia Techen
pubs.organisational-group/Virginia Tech/Engineeringen
pubs.organisational-group/Virginia Tech/Engineering/Biomedical Engineering and Mechanicsen
pubs.organisational-group/Virginia Tech/Faculty of Health Sciencesen
pubs.organisational-group/Virginia Tech/All T&R Facultyen
pubs.organisational-group/Virginia Tech/Engineering/COE T&R Facultyen

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